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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Personal experience in the management of three cases of primary hyperaldosteronism, in which a cure was obtained by surgical removal of an adrenocortical adenoma, is was used in the elaboration of a diagnostic procedure requiring hospitalisation for 12 days. During 6 days, the patient is kept on a diet containing 100 mEq Na and K, and blood potassium values are repeatedly determined. Other causes of hypertension are ruled out. On the 6th day, baselines for blood renin and urinary aldosterone are calculated. Next, a hyposodic diet is given for 4 days, and a diuretic is administered on the last of these days, after which renin is determined "in response to stimulation". Lastly, two days of i.v. NaCl loading are followed by the determination of urinary aldosterone "during inhibition". If the picture is positive for hyperaldosteronism, the patient is discharged and followed during treatment with spironolactone, and eventually subjected to renal and adrenal arteriography to determine the site of the adenoma. Division of the procedure into increasingly complex steps enables the examination to be halted at any point when evidence in support of the suspected diagnosis fails to appear. This feature, coupled with the simplicity of the procedures adopted, enables all young subjects admitted for unexplained hypertension to be screened for hyperaldosteronism, with the assurance of obtaining certain diagnosis without an excessively long stay in hospital.
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PMID:[Primary hyperaldosteronism. Diagnostic procedure useful in hospital routine]. 63 79

To study whether the renin-angiotensin system is related to hyperuricemia in hypertension, the serum concentration of uric acid was determined in 96 patients with various types of hypertension and various degrees of plasma renin activity (PRA). In malignant hypertension, both PRA and the serum uric acid level were higher than in essential hypertension; but in primary aldosteronism or desoxycorticosterone-excess hypertension, they were lower than in the essential type. In renovascular hypertension, PRA was higher than in essential hypertension, but the serum uric acid levels were similar. There were no differences in PRA and serum uric acid concentration between Cushing's syndrome and essential hypertension. The serum uric acid level in high-renin essential hypertension was higher than in either the normal-renin or the low-renin type. There was a significant correlation between serum uric acid concentration and PRA in the basal state, and between the change in PRA and the change in serum uric acid induced by administration of furosemide. Apparently the close correlation between the renin-angiotensin system and the concentration of serum uric acid is related to changes in extracellular fluid volume, although an intrarenal effect of angiotensin II cannot be excluded.
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PMID:Serum uric acid and the renin-angiotensin system in hypertension. 65 66

A method for simultaneous measurement of 11-deoxycorticosterone (DOC), 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) and aldosterone using 1.0-2.0 ml of plasma has been developed. The present method consists of extracting plasma with dichloromethane, separating the DOC, 18-OH-DOC, and aldosterone from other steroids on a Sephadex LH-20 column, and quantitating each steroid by radioimmunoassay. This method was demonstrated to be sensitive, accurate and precise. In 20 normal male subjects, the mean recumbent level of DOC was 9.1 +/- 3.1 ng/100 ml, on random diet, at 0800 h. The corresponding levels of 18-OH-DOC and aldosterone were 8.2 +/- 3.9 ng/100 ml, and 6.7 +/- 2.6 ng/100 ml, respectively. Plasma levels of these three steroids were measured in several types of adrenocortical disorders associated with hypertension and hypokalemia. Patients with Cushing's syndrome due to adrenocortical hyperplasia, and 17alpha-hydroxylase deficiency had elevated DOC and 18-OH-DOC levels, but showed normal or lower aldosterone levels. Hypersecretion of DOC and 18-OH-DOC may cause the symptoms of hypertension and hypokalemia. Patients with primary aldosteronism had elevated levels of DOC and 18-OH-DOC as well as aldosterone. The former two steroids may be hyperproduced as a precursor of aldosterone.
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PMID:Simultaneous determination of plasma 11-deoxycorticosterone, 18-hydroxy-11-deoxycorticosterone, and aldosterone in man. 66 34

1. The 24 h urinary excretion of kallikrein has been studied in 40 normotensive control subjects and in 74 age-matched patients with essential hypertension under similar conditions. By use of the renin-sodium index, hypertensive patients were divided into two subgroup: low-renin hypertension and normal-renin hypertension patients. Urinary kallikrein determinations were also obtained from six hypertensive patients with primary aldosteronism. 2. Urinary kallikrein was significantly lower both in patients with normal-renin and low-renin essential hypertension. Urinary kallikrein excretion was very high in the patients with primary aldosteronism. 3. In nine hypertensive patients beta-adreno-receptor-blocking therapy caused a significant decrease of plasma renin activity, but had no significant effect on urinary kallikrein excretion. 4. The results support the concept that low urinary kallikrein is likely to be a marker of essential hypertension. Under certain conditions its excretion is positively related to mineralocorticoid hormone concentrations but it is not primarily related to the renin-angiotensin system.
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PMID:Urinary kallikrein excretion and plasma renin activity in patients with essential hypertension and primary aldosteronism. 66 67

Hypokalemia is an uncommon cause of rhabdomyolysis with acute tubular necrosis. We recently treated a patient in whom severe hypokalemia attributed to diuretic therapy antedated acute myoglobinuric renal failure by six months. After recovery, hypokalemia persisted and subsequent evaluation disclosed primary aldosteronism. This case is a unique presentation for primary aldosteronism and illustrates the importance of diagnosis before treatment in hypertension as well as the hazards of hypokalemia.
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PMID:Primary aldosteronism presenting as myoglobinuric acute renal failure. 68 40

Twenty-two cases with essential arterial hypertension were studied in the final part of a chronic period of treatment with Chlortalidona and in the first 30 days after treatment. Measurements of the following parameters were made: 1) Change in the excretion of urinary aldosterone (aldo). 2) Change in the arterial pressure (delta P). 3) Transtherapeutic serum potassium (delta K). 4) Change in the Q-T (delta QT) in the electrocardiogram. The measurements were made 3 days after the suppression of the drug and afterwards every 3 to 6 days for a month. The correlation of the K and QT was significant (r = 0.63). The P did not correlate with the K nor with the aldo (r = 0.14). The aldo was -5.92 +/- 3.1 ug./24 hs (p = 0.01) in those cases responsive to the drug. The disappearance of the antihypertensive effect occurred at 9.61 +/- 3.7 days and correlated with the normalization of the QT (r = 0.83) and the serum potassium. The delta aldo correlated with K (r = 0.56) and normalized 6.7 days after the suspension of the drug. The secondary aldosteronism participates in the parogenia of the transtherapeutic hypokalemia although with a slightly significant correlation. The important correlation between the disappearances of the antihypertensive effects and the electrocardiographic signs of hypokalemia may dwell in changes which directly or indirectly exercise the diuretic in the intracellular metabolism of K without necessarily cousing an antihypertensive effect additive of the same hypokalemia.
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PMID:[Aldosteronism after hypokalemia in diuretic therapy of systemic arterial hypertension]. 69 72

In order to evaluate the relationship between aldosterone status and the blood pressure-lowering effect of spironolactone, 38 patients with essential hypertension were treated with spironolactone (400 mg/day) during one week in hospital on a rigidly sodium-restricted diet. The degree of hyperaldosteronism was assessed by the aldosterone secretory rate after 5 days of salt loading (315 mmol Na+/day). The mean arterial pressure decreased 5.6% (range, -21 to +8%). When the patients were divided into subgroups with low and normal renin activity, there was no difference in the change in mean arterial pressure (-5.0% and -6.1%). When the patients were divided into three groups with low, normal, and supranormal aldosterone secretory rates, the last group had a significantly greater fall in blood pressure after the spironolactone than the other groups (-1.0, -7.1, -11.1%). Thus there was a correlation between the aldosterone secretory rate after sodium loading and the blood pressure-lowering effect of spironolactone (r = -0.53, p less than 0.01). The blood pressure-lowering effect was not related to changes in body weight, kidney function, or plasma electrolytes. Our findings do not provide solid arguments for the view that the blood pressure-lowering effect of high dose spironolactone is due to its antimineralocorticoid activity, but the correlation between the degree of hyperaldosteronism and the blood pressure-lowering effect strongly suggests that aldosterone does play a role in the genesis or maintenance of the hypertension in these patients.
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PMID:Role of aldosterone in the antihypertensive effect of spironolactone in essential hypertension. 71 23

Two cases are reported of a 30-year-old and of a 28-year-old Japanese women with primary aldosteronism in whom metabolic and blood pressure abnormalities were aggravated during peripartum period. The characteristic findings in 2 present cases are as follows; 1) lower blood pressure during pregnancy, 2) elevated blood pressure during peripartum period, and 3) after parturition, serum potassium decreased, and the blood pressure elevated. The reason why the hypertension and hypokalemia associated with primary aldosteronism were ameliorated during pregnancy was thought to be due to the increased secretion of progesterone. Furthermore, the rapid recurrence of symptoms, increase in blood pressure, and hypokalemia in the post-partum period could be related to elevated prolactin and decreased progesterone levels.
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PMID:Primary aldosteronism aggravated during peripartum period. 75 Jun 75

Plasma volume is usually lower in patients with essential hypertension than in normal subjects. Normal or expanded plasma volume in some hypertensive patients may respect either a specific hypervolemic subset of the disease or the upper end of a continuum of volume values. Difficulties in defining these groups stem from the small numbers of subjects studied, from the need for a reliable reference index for volume measurements, and from the multiple factors which may affect intravascular volume. Differences in plasma volume cap influence choice of antihypertensive therapy; patients with expanded volume tend also to have slightly exchangeable sodium and greater extracellular fluid (ECF) volume and to respond well to diuretic therapy. There is also some evidence that low plasma renin activity is more frequent among hypervolemic patients. Essential hypertensives as a group have low plasma to interstitial fluid volume ratio (PV/IF), indicating that ECF distribution between the intravascular and interstitial compartments is shifted toward the latter. This is probably related to altered capillary filtration pressure due to increased venous resistance. Hypovolemic essential hypertensives have significantly lower (P less than 0.01) PV/IF ratio than hypervolemic, but whether this is related to differences in neural venous tone is only speculative. Hemodynamic studies revealed no difference in cardiac output between hypertensive patients with contracted blood volume and those with hypervolemia; total peripheral resistance was even higher in the latter, suggesting that "vasoconstriction" is not different between the two groups. It is widely believed that the relationship between ECF expansion and hypertension depends on the development of hypervolemia, increased cardiac output, and subsequent rise in total peripheral resistance reducing volume expansion and normalizing systemic flow while maintaining a high blood pressure. This sequence of events has been demonstrated in some human and experimental forms of hypertension but not in all. Metyrapone-induced hypertension in dogs could be sustained for up to 6 weeks by increased output with no evidence of "autoregulation" developing, and similar observations were reported in some anephric patients. Complementing these findings are observations of elevated cardiac output in some patients with long-standing essential hypertension or primary aldosteronism. It is therefore suggested that the spectrum of hemodynamic changes associated with volume disturbances in hypertension is too wide to be forced under one hypothesis alone and that neurogenic and other factors may play an important role in that complex relationship.
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PMID:Hemodynamic role of extracellular fluid in hypertension. 77 71

Aspirin has been shown to acutely block the natriuretic effect of spironolactone in the mineralocorticoid-treated normal rat, dog, and man. It has been suggested that aspirin is contraindicated in hypertensive patients receiving spironolactone. Five patients with low-renin essential hypertension and two with hypertension due to primary aldosteronism, all of whom have normalized their blood pressure on chronic spironolactone therapy, were cotreated in a double-blind fashion with either aspirin or aspirin-placebo during alternate six-week periods. Aspirin did not appear to alter the effect of spironolactone on blood pressure, serum electrolytes, urea nitrogen, or plasma renin activity.
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PMID:Failure of aspirin to antagonize the antihypertensive effect of spironolactone in low-renin hypertension. 78 8


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